Hey all!!
if you haven’t followed the threads i’ve posted in let me fill you in.
i am 59, stage 3 grade 3, genotype 2. i started TX in march '08 and by week 2 was UD with normal liver function. I completed tx in sept. '08. it was a very tough summer and i’m still waiting for the side effects to stop. i just had my 1st post TX tests and i’m glad to say i still have normal liver function (alt / ast) and still UD virla load. my hepatologist christened me SVR and said I COULD LOOK FORWARD TO MY LIVER STARTING TO HEAL ITSELF. it feels great to be on this side of the whole experience. i will post a more detailed account in my journal.
the reason for this thread is to share with everyone, especially those trying to decide to do treatment or not, two studies posted on the Hepatitis Association web site:
if you want to read them on the site they are posted in links on the right side of the home page.
i would be greatly interested in your feed back.
Liver Biopsies Indicate Persistent Inflammation and Fibrosis in HCV Antibody Positive People with Undetectable HCV RNA
December 2008
People who carry antibodies indicating exposure to hepatitis C virus (HCV), but who have undetectable plasma HCV viral load, are generally considered to have inactive disease. Likewise, continued undetectable plasma HCV RNA 24 months after completion of interferon-based therapy is usually regarded as a cure.
But hidden HCV in the liver – even in the absence of detectable virus in the blood – may still lead to liver disease progression, according to a study published in the December 2008 issue of Hepatology.
It is unclear whether HCV has been eradicated or persists at a low level in HCV antibody positive HCV RNA negative individuals, the study authors noted as background, and the natural history of the disease and liver histology in such individuals are not well characterized.
Matthew Hoare and colleagues from the U.K. studied 172 HCV antibody positive but plasma HCV RNA negative individuals who underwent diagnostic liver biopsies between 1992 and 2000. A total of 102 patients who had any possible causes of liver injury other than HCV were excluded. The remaining 70 participants were analyzed after a median 7 (range 5-12) years of follow-up.
A single pathologist scored biopsy samples according to the Ishak scoring criteria. Characterization of inflammatory infiltrate in selected patients was done using a novel semi-quantitative technique, and results were compared with those of patients with detectable HCV RNA and HCV antibody negative healthy control subjects.
Results
4 of the 70 patients (5.7%) became HCV RNA positive during follow-up.
66 patients (94.3%) remained HCV RNA negative.
5 patients (7.5%) had normal liver biopsies.
54 of the patients with abnormal biopsies (82%) had liver fibrosis, including 16 (24%) with moderate to advanced (stage 2 or 3) fibrosis.
Biopsies from patients with undetectable plasma HCV RNA revealed expanded portal tracts with fewer CD4 cells and more CD8 cells than healthy HCV negative control subjects, but indistinguishable from patients with detectable plasma HCV RNA.
Lobular CD4 staining was absent in control subjects, but present in patients with both undetectable and detectable plasma HCV RNA (more marked in the latter).
“Non-viremic HCV antibody positive patients have a liver biopsy that is usually abnormal,” the study authors conclude. “Fibrosis was present in most with similar inflammatory infiltrate to viremic cases.”
The added that, “The presence of a CD8 rich inflammatory infiltrate suggests an ongoing immune response in the liver, supporting the view that HCV may persist in the liver in the majority of HCV RNA negative cases.”
Department of Medicine, School of Clinical Medicine, University of Cambridge, Cambridge, UK; Department of Pathology, University of Cambridge, Cambridge, UK; Clinical Microbiology and Public Health Laboratory, Health Protection Agency, Addenbrooke’s Hospital, Cambridge, UK; Medical Research Council (MRC) Cancer Cell Unit, Hutchison/MRC Research Centre, Cambridge, UK.
M Hoare, WT Gelson, SM Rushbrook, and others. Histological changes in HCV antibody-positive, HCV RNA-negative subjects suggest persistent virus infection. Hepatology. 48(6): 1737-1745. December 2008. (Abstract).
Although Hepatitis C Treatment Reduces The Virus, Liver Damage Continues
10 Dec 2008
Treating patients who have chronic hepatitis C and advanced liver disease with long-term pegylated interferon significantly decreased their liver enzymes, viral levels and liver inflammation, but the treatment did not slow or prevent the progression of serious liver disease, a study finds.
These findings come from the clinical trial, Hepatitis C Antiviral Long-Term Treatment Against Cirrhosis (HALT-C) and are reported in the Dec. 4 issue of the New England Journal of Medicine. HALT-C was funded by the National Institutes of Health (NIH) with additional support from Hoffmann-La Roche Inc.
“The results from HALT- C show without question that maintenance therapy with peginterferon does not prevent progression of liver disease among patients who have failed prior treatments,” said James Everhart, M.D., project scientist for HALT-C in the Division of Digestive Diseases and Nutrition, National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), the principal sponsor of HALT-C at NIH. “These findings heighten the incentive to develop more effective drugs for patients with severe liver disease due to hepatitis C.”
Peginterferon therapy for up to 48 weeks is standard for chronic hepatitis C. But patients who do not have a sustained response to initial therapy have been given the drug over a longer time based on studies showing that this approach suppresses viral and enzyme levels, even if the virus is not completely eliminated. However, it was not known if long-term therapy would improve important clinical outcomes such as liver damage and death.
HALT-C, a randomized multicenter trial of 1,050 patients with chronic hepatitis C who had failed prior treatment to eradicate the infection, tested whether long-term treatment with peginterferon alfa-2a would reduce the development of cirrhosis, liver cancer, or liver failure. The 517 patients randomized to the treatment arm received 90 micrograms of peginterferon in weekly injections for 3.5 years. The 533 patients in the control arm underwent the same follow-up and care as the treated patients including liver biopsies, quarterly clinic visits and blood tests. All patients had advanced liver fibrosis, a gradual scarring of the liver that puts patients at risk for progressive liver disease and liver failure.
The outcomes studied in HALT-C were death, liver cancer, or liver failure, and for those who did not have cirrhosis initially, the development of cirrhosis. At the end of the study, 34.1 percent of the treated group and 33.8 percent of the control group had experienced at least one outcome. Patients in the treated group had significantly lower blood levels of the hepatitis C virus and improvement in liver inflammation. However, there was no major difference in rates of any of the primary outcomes between the groups.
Among treated patients, 17 percent stopped peginterferon after 18 months and 30 percent stopped the drug after two years. Infections, musculoskeletal or digestive problems were the most common reasons for stopping the drug.
According to HALT-C study chair and principal investigator Adrian M. Di Bisceglie, M.D., professor of internal medicine at Saint Louis University School of Medicine in Missouri, looking into how maintenance therapy works in non-responders is an important step. “Patients should not receive interferon as maintenance therapy for chronic hepatitis C. However, we can build on what was learned in HALT-C to identify better treatments that may delay or prevent liver damage in patients with advanced disease,” he said.
Article adapted by Medical News Today from original press release.
The hepatitis C virus infects more than 100 million persons worldwide and as many as 4 million in the United States. Hepatitis C ranks with alcohol abuse as the most common cause of chronic liver disease and leads to about 1,000 liver transplants in the United States each year. The best current antiviral therapy of pegylated interferon given by injection in combination with oral ribavirin for about 6 months to a year eliminates the virus in about 50 percent of infected patients.
The following researchers and clinical centers conducted the HALT-C study:
Dr. Jules L. Dienstag, Massachusetts General Hospital and Harvard Medical School, Boston, Mass.
Dr. Adrian M. Di Bisceglie (Study Chair), Saint Louis University School of Medicine, Saint Louis, Mo.
Dr. Anna S. Lok, University of Michigan Medical Center, Ann Arbor
Dr. Gyongyi Szabo, University of Massachusetts, Worcester
Dr. Timothy R. Morgan, University of California, Irvine and VA Long Beach Healthcare System, Long Beach, Calif.
Gregory T. Everson, University of Colorado Health Sciences Center, Denver
Dr. Herbert L. Bonkovsky, University of Connecticut Health Center, Farmington.
Dr. Karen L. Lindsay, Keck School of Medicine, University of Southern California, Los Angeles
Dr. William M. Lee, University of Texas Southwestern Medical Center, Dallas
Dr. Mitchell L. Shiffman, Virginia Commonwealth University Medical Center, Richmond
Dr. Chihiro Morishima and Dr. David Gretch, University of Washington, Seattle
Dr. Kristin K. Snow, New England Research Institutes, Watertown, Mass.
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